Langerhans Cell Density in Cervical Intraepithelial Neoplasia Associated With Human Papillomavirus Infection in HIV-Infected and HIV-Noninfected Brazilian Women

*School of Medicine, Federal University of Juiz de Fora
International Journal of Gynecological Cancer (Impact Factor: 1.95). 08/2012; 22(8):1291-6. DOI: 10.1097/IGC.0b013e318263ef88
Source: PubMed


Local immunity plays an important role in the cervical defense mechanisms that prevent the development of cervical intraepithelial neoplasia. The objective of this study was to determine the involvement of local immunity by evaluating Langerhans cell (LC) density in cervical biopsies of human immunodeficiency virus (HIV)-positive and HIV-negative women.
A cross-sectional study was developed by including HIV-positive and HIV-negative women. All patients presented human papillomavirus DNA from the uterine cervix, which was detected by polymerase chain reaction or hybrid capture II. Cervical biopsies were assessed for LC density and cervical intraepithelial neoplasia. Langerhans cells were identified by immunohistochemistry using anti-CD1a and anti-S100 antibodies. Associations among cervical LC density, the type of cervical lesion, CD4 lymphocyte count, and HIV viral load were analyzed using logistic regression (SPSS, version 12.0).
Seventy-seven women (40 seropositive and 37 seronegative) were enrolled. The mean ± SD LC density identified with the anti-CD1a antibody was 0.80 ± 0.7 cells versus 2.6 ± 1.6 cells (P < 0.0001), whereas the mean ± SD LC density identified by the anti-S100 antibody was 1.3 ± 1.0 cells versus 3.6 ± 1.7 cells (P < 0.0001) among the HIV-positive and HIV-negative women, respectively. There were no associations between LC density and HIV viral load, CD4 lymphocyte count, or human papillomavirus genotype (P > 0.05). In a logistic regression model, HIV infection was the only factor independently associated with a decrease in LC density.
Human immunodeficiency virus infection was found to be an independent factor that explains the decrease in local immunity in the uterine cervix, which could allow the development of cervical lesions. This effect was not associated with CD4 lymphocyte count or HIV viral load.

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    ABSTRACT: Cervical intraepithelial neoplasias (CIN) are closely associated with oncogenic subtypes of the human papillomavirus (HPV). In the presence of this virus, it is known that the activation or suppression of immune system is the key to the development, progression and/or regression of cervical lesions. Therefore, the objective of this study is to compare the local immune response among HIV-seropositive and seronegative patients with cervical intraepithelial neoplasia regarding the expression of T lymphocytes (CD3+, CD4+ and CD8+), B lymphocytes (CD20+) and natural killers cells (CD56+) in the cervical stroma. A cross-sectional study of paraffin blocks containing cervical tissue after conization by the Loop Electrosurgical Excision Procedure (LEEP) from 47HIV-seropositive and 38 seronegative patients with CIN. Cervical stroma immunohistochemistry was performed in the CIN area. The Fisher's exact test was used for the statistical analysis. When HIV-seropositive and seronegative women were compared, the seropositive women had a higher count of CD8+ T lymphocytes (52.1% versus 28.9%, P<0.04). Considering CIN degree (CIN 1 and CIN 2/3), the HIV-seronegative patients with CIN 1 had a low count of CD20+B-lymphocytes (7.1%) in comparison with CIN 1HIV seropositive and with CIN 2/3HIV-seronegative patients, respectively 50% (P< 0.018) and 54.5% (P< 0.0048). The HIV infection and degree of CIN influenced the cytotoxic lymphocytes inducing an increase in the number of cells high count of CD20+ lymphocytes with CIN 1.
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